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Health & Medicine for Senior Citizens

Aspirin, Painkillers Ward Off Skin Cancer; Second Study Lets Immune System Stop Melanoma

NSAIDs decreased risk for squamous cell carcinoma and malignant melanoma; advanced melanoma patients see scientist lower cancer barrier to allow immune system attack

Novel treatment exposes melanoma to successful immune system attack.

May 29, 2012 - Senior citizens – the major targets of skin cancers – received significant good news from two sources in the last few days. A study released today says aspirin and other painkillers appear to offer protection from skin cancer. Another study out a week ago found a means of allowing the immune system to attack melanoma skin cancers and causing them to stabilize or recede in half those in the clinical trial.

Today’s study published early online in CANCER, a peer-reviewed journal of the American Cancer Society, suggests that skin cancer prevention may be added to the benefits of the commonly used aspiring and other painkilling medications. Other recent studies have indicated a cancer-fighting ability of aspirin (see links in sidebar).


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Previous have indicated that taking nonsteroidal anti-inflammatory drugs, or NSAIDs, which include aspirin, ibuprofen, and naproxen, as well as a variety of other nonprescription and prescription drugs, can decrease an individual’s risk of developing some types of cancer.

But Denmark researchers from Aarhus University Hospital, led by Sigrún Alba Jóhannesdóttir, BSc, looked to see if the medications might decrease the risk of the three major types of skin cancer: basal cell carcinoma, squamous cell carcinoma, and malignant melanoma.

The researchers analyzed medical records from northern Denmark from 1991 through 2009 and identified 1,974 diagnoses of squamous cell carcinoma, 13,316 diagnoses of basal cell carcinoma, and 3,242 diagnoses of malignant melanoma. They compared information, including prescription data, from these patients with information from 178,655 individuals without skin cancer.

Individuals who filled more than two prescriptions for NSAIDs had a 15 percent decreased risk for developing squamous cell carcinoma and a 13 percent decreased risk for developing malignant melanoma than those who filled two or fewer prescriptions for the medications, especially when the drugs were taken for seven or more years or taken at high intensity.

Individuals who took NSAIDs did not seem to benefit from a reduced risk of developing basal cell carcinoma in general, although they did have a 15 percent and 21 percent reduced risk of developing this type of cancer on less-exposed sites (body areas other than the head and neck) when they took them long term or at high intensity, respectively.

“We hope that the potential cancer-protective effect of NSAIDs will inspire more research on skin cancer prevention,” said Ms. Jóhannesdóttir. “Also, this potential cancer-protective effect should be taken into account when discussing benefits and harms of NSAID use.”

Novel treatment exposes melanoma to immune system attack

The study released on May 23, found that antibodies that lower cancer's guard against an immune system attack caused melanoma growths to recede or stabilize in half of patients who took part in a clinical trial of the therapy at Dana-Farber Cancer Institute.

The scientists will report on the study at the annual meeting of the American Society of Clinical Oncology (ASCO) June 1-5 in Chicago.

The phase I trial involved 104 patients with advanced melanoma, a skin cancer that can become lethal if it spreads to other parts of the body. The patients were treated with a monoclonal antibody — a preparation of millions of identical proteins — that rescinds a "Halt!" order on T cells' attack on melanoma cells.

The antibody targets a receptor called PD-1 on the surface of T cells. In doing so, it targets the interaction between PD-1 and a companion protein, or ligand, called PD-L1. The interaction of PD-1/PD-L1 shuts down T cells' attack on melanoma; blocking that interaction allows the attack to resume.

"The interaction of PD-1 and PD-L1 essentially stiff-arms the immune system from attacking melanoma," says the lead author of the ASCO study, F. Stephen Hodi, MD, director of the Center for Melanoma Oncology at Dana-Farber. "Blocking that interaction allows the immune system to proceed with the attack. It lets the T cells do their job."

Hodi will present the data (abstract 8507) in an oral session on Monday, June 4, 8 a.m. CT, in the Arie Crown Theater, McCormick Place. Hodi also has provided video commentary on the findings.

Patients participating in the trial received the antibody preparation, known as BMS-936558, for up to two years. Side effects were for the most part minor.

Although the phase I trial is now closed, researchers hope to begin phase II and III studies of the approach later this year.

The research builds on earlier work by Dana-Farber's Gordon Freeman, PhD, and others who identified the PD-L1 ligand on tumor cells and showed how the interaction between PD-1 and PD-L1 can turn off the immune response to cancer. Freeman and his colleagues were also the first to show how monoclonal antibodies could be used to reactivate the immune response.

In addition to Hodi, the study's other authors are Mario Sznol, MD, Yale Cancer Center, New Haven, CT; David F. McDermott, MD, Beth Israel Deaconess Medical Center, Boston; Richard D. Carvajal, MD, Memorial Sloan-Kettering Cancer Center, New York; Donald P. Lawrence, MD, Massachusetts General Hospital Cancer Center, Boston; Suzanne Louise Topalian, MD, Johns Hopkins University School of Medicine, Baltimore, MD; Jon Wigginton, MD, Dan McDonald, Georgia Kollia, PhD, and Ashok Kumar Gupta, PhD, Bristol-Myers Squibb, Princeton, NJ; and Jeffrey Alan Sosman, MD, Vanderbilt University Medical Center, Nashville, TN.

The study was funded by Bristol-Myers-Squibb.


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